Bin Wang1,2,3, Mian Li1,2,3, Zhiyun Zhao1,2,3, Jieli Lu1,2,3, Yuhong Chen1,2,3, Yu Xu1,2,3, Min Xu1,2,3, Weiqing Wang1,2,3, Tiange Wang4,5,6, Yufang Bi7,8,9, Guang Ning1,2,3. 1. State Key Laboratory of Medical Genomics, Key Laboratory for Endocrine and Metabolic Diseases of Ministry of Health, National Clinical Research Center for Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai, 200025, China. 2. Department of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 3. Shanghai Institute of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 4. State Key Laboratory of Medical Genomics, Key Laboratory for Endocrine and Metabolic Diseases of Ministry of Health, National Clinical Research Center for Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai, 200025, China. wtg@live.cn. 5. Department of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. wtg@live.cn. 6. Shanghai Institute of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. wtg@live.cn. 7. State Key Laboratory of Medical Genomics, Key Laboratory for Endocrine and Metabolic Diseases of Ministry of Health, National Clinical Research Center for Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai, 200025, China. byf10784@rjh.com.cn. 8. Department of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. byf10784@rjh.com.cn. 9. Shanghai Institute of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. byf10784@rjh.com.cn.
Abstract
AIMS/HYPOTHESIS: Bisphenol A (BPA) has been shown to be potentially associated with type 2 diabetes; however, there is little evidence associating BPA exposure with glucose metabolic outcomes prior to diabetes onset. We aimed to examine BPA exposure in relation to glucose homeostasis among non-diabetic individuals. METHODS: This longitudinal cohort study comprised 2336 Chinese adults aged 40 years or above (62.8% women) and free of diabetes at baseline in 2009, followed for 4 years. Urinary BPA and glucose metabolic traits including fasting plasma glucose (FPG), 2 h post-load plasma glucose, fasting serum insulin, HOMA-IR and HOMA-B were measured at baseline and follow-up. Repeated-measures analysis was performed to evaluate associations of urinary BPA concentration with markers of glucose homeostasis. RESULTS: After full adjustment for confounders including BMI, each tenfold increase in urinary BPA concentrations was associated with a 3.39% increase in FPG (95% CI 2.24%, 4.55%) and an 11.6% decrease in HOMA-B (95% CI -15.8%, -7.18%) in women. The inverse association between urinary BPA and HOMA-B was more prominent among overweight or obese individuals (change -13.7%; 95% CI -19.3%, -7.61%) compared with those who were of normal weight (change -6.74%; 95% CI -13.2%, 0.20%) (pinteraction = 0.07). Moreover, the ORs of fasting hyperglycaemia and beta cell dysfunction corresponding to a tenfold increase in urinary BPA concentrations were 1.37 (95% CI 1.10, 1.72) and 1.30 (95% CI 1.02, 1.65) in women, respectively. No significant associations existed between urinary BPA and glucose metabolic markers in men. CONCLUSIONS/ INTERPRETATION: Our findings suggest that exposure to BPA was independently associated with impaired glucose homeostasis before the development of diabetes in middle-aged and elderly women.
AIMS/HYPOTHESIS: Bisphenol A (BPA) has been shown to be potentially associated with type 2 diabetes; however, there is little evidence associating BPA exposure with glucose metabolic outcomes prior to diabetes onset. We aimed to examine BPA exposure in relation to glucose homeostasis among non-diabetic individuals. METHODS: This longitudinal cohort study comprised 2336 Chinese adults aged 40 years or above (62.8% women) and free of diabetes at baseline in 2009, followed for 4 years. Urinary BPA and glucose metabolic traits including fasting plasma glucose (FPG), 2 h post-load plasma glucose, fasting serum insulin, HOMA-IR and HOMA-B were measured at baseline and follow-up. Repeated-measures analysis was performed to evaluate associations of urinary BPA concentration with markers of glucose homeostasis. RESULTS: After full adjustment for confounders including BMI, each tenfold increase in urinary BPA concentrations was associated with a 3.39% increase in FPG (95% CI 2.24%, 4.55%) and an 11.6% decrease in HOMA-B (95% CI -15.8%, -7.18%) in women. The inverse association between urinary BPA and HOMA-B was more prominent among overweight or obese individuals (change -13.7%; 95% CI -19.3%, -7.61%) compared with those who were of normal weight (change -6.74%; 95% CI -13.2%, 0.20%) (pinteraction = 0.07). Moreover, the ORs of fasting hyperglycaemia and beta cell dysfunction corresponding to a tenfold increase in urinary BPA concentrations were 1.37 (95% CI 1.10, 1.72) and 1.30 (95% CI 1.02, 1.65) in women, respectively. No significant associations existed between urinary BPA and glucose metabolic markers in men. CONCLUSIONS/ INTERPRETATION: Our findings suggest that exposure to BPA was independently associated with impaired glucose homeostasis before the development of diabetes in middle-aged and elderly women.
Authors: Jong-Joo Kim; Surendra Kumar; Vinay Kumar; Yun-Mi Lee; You-Sam Kim; Vijay Kumar Journal: Int J Environ Res Public Health Date: 2019-12-22 Impact factor: 3.390
Authors: Francesca Farrugia; Alexia Aquilina; Josanne Vassallo; Nikolai Paul Pace Journal: Int J Environ Res Public Health Date: 2021-01-15 Impact factor: 3.390